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S-allylcysteine induces cell cycle arrest and apoptosis in androgen-independent human prostate cancer cells.
Liu, Zhuo; Li, Mingchao; Chen, Ke; Yang, Jun; Chen, Ruibao; Wang, Tao; Liu, Jihong; Yang, Weimin; Ye, Zhangqun.
Afiliação
  • Liu Z; Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, PR China.
Mol Med Rep ; 5(2): 439-43, 2012 02.
Article em En | MEDLINE | ID: mdl-22052207
To increase the use of phytochemical supplements as chemoprevention or adjuvant drugs in cancer treatment, it is necessary to verify their biological effects and correlative mechanisms. Recently, S-allylcysteine (SAC) was identified as a potent compound derived from garlic. The aim of this study was to evaluate the anticancer effects of SAC on androgen-independent human prostate cancer (PC-3) cells and to elucidate the possible mechanisms. PC-3 cells were incubated with SAC at three different concentrations. Cell growth was determined by Cell Counting Kit-8 and 5-ethynyl-2'-deoxyuridine assay. Cell cycle and apoptosis were determined by flow cytometric assay. The expression of apoptosis-related molecules was detected by Western blot analysis. We found that SAC suppressed the proliferation of PC-3 cells and led to cell cycle arrest at the G0/G1 phases, as well as inducing cell apoptosis which was accompanied by the decreased expression of Bcl-2 and increased expression of Bax and caspase 8. This study demonstrated the chemopreventive activity of SAC in vitro, and that SAC may be a promising candidate for prostate cancer treatment.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Apoptose / Cisteína / Pontos de Checagem do Ciclo Celular / Androgênios / Antineoplásicos Idioma: En Revista: Mol Med Rep Ano de publicação: 2012 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Apoptose / Cisteína / Pontos de Checagem do Ciclo Celular / Androgênios / Antineoplásicos Idioma: En Revista: Mol Med Rep Ano de publicação: 2012 Tipo de documento: Article